Thoru Yamada

Investigating the Relationship Between Stroke and Obstructive Sleep Apnea

BACKGROUND AND PURPOSE We aimed to prospectively determine whether the incidence of obstructive sleep apnea in patients with recent stroke was significantly different from that of a sex- and age-matched control group with no major medical problems. METHODS We prospectively performed overnight polysomnography in 24 patients with a recent stroke (13 men and 11 women; mean age [+/- SD], 64.6 +/- 10.4 years) and 27 subjects without stroke (13 men and 14 women; mean age, 61.6 +/- 8.8 years). Patients with either ischemic or hemorrhagic stroke were entered into this study. Polysomnographic evaluations were performed within approximately 2 to 5 weeks after each patients stroke. RESULTS Obstructive sleep apnea was found in 10 of 13 men with stroke (77%) and in only 3 of 13 male subjects without stroke (23%) (P=.0169). Seven of 11 women with stroke (64%) had obstructive sleep apnea, while only 2 of 14 female subjects without stroke (14%) had obstructive sleep apnea (P=.0168). For men with stroke, the mean apnea/hypopnea index (+/- SE) was 21.5 +/- 4.2 events per hour, while for male subjects without stroke it was 4.8 +/- 1.8 events per hour (P=.0014). For women with stroke the mean apnea/hypopnea index was 31.6 +/- 8.8 events per hour, while for female subjects without stroke it was 2.9 +/- 1.6 events per hour (P=.0024). The 4-year mortality for patients with stroke was 20.8%. All patients with stroke who died had obstructive sleep apnea. CONCLUSIONS Patients with stroke have an increased incidence of obstructive sleep apnea compared with normal sex- and age-matched control subjects. Hypoxia and hemodynamic responses to obstructive sleep apnea may have predisposed these patients to stroke.

An Experimental Study in Chickens for the Pathogenesis of Idiopathic Scoliosis

Experimentaliy induced scoliosis was investigated in pinealectomized chickens using pathologic and neurophysiologic means. A total of 90 chickens were tested; 30 served as a normal control 30 received an autografted pineal body in the intramuscular tissue of the trunk, and 30 underwent pinealectomy without autograft. Scoliosis developed in all pineslectomized chickens within 2 weeks, showing gradual progression during the next 5 or 6 weeks. At 3 months, the three-dimensional spinal deformity consisted of lateral curvature and vertebral body rotation, resulting in a praminent lordoscoliosis at the thoracic level. In contrast, scoliosis developed in only 10% of the autagrafted chickens. Histologic examination revealed no pathologic change in the brain in either the pinealectomized scoliosis group or in the autografted nonscoliosis group. Cortical potentials in the scoliosis group were delayed, thus suggesting conduction disturbance rostral to the brain stem. Although the relationship between the cause and effect is uncertain, these findings implicate neurotransmitters or neurohormonal systems in the pineal body as a major contributing factor in this type of axperimental scoliosis.

Short latency somatosensory evoked potentials following median nerve stimulation in man

Abstract In 20 normal subjects, short latency components of the somatosensory evoked potentials (SEPs) were recorded simultaneously from the scalp and cervical electrodes after stimulation of the median nerve at the wrist. Using a knee reference, 4 positive peaks, P9, P11, P13 and P14, were identified in the scalp recorded potentials, whereas the cervical potentials consisted of the initial positive peak, Pc9, and 3 subsequent negative peaks, N11, N13 and N14. The initial component was negative over the shoulder but otherwise distributed widely as a positive field from the neck to the scalp. Its latency was slightly less than that of the nerve potential recorded at Erbs point. The second component was best recorded at the low cervical area as a negative peak, increasing in amplitude and decreasing in latency laterally towards the site of the stimulus. Its latency was nearly the same as an estimated nerve conduction time from the wrist to the spinal cord. The third component was most consistently recorded as a negative peak at mid and low cervical electrodes, progressively decreasing in amplitude toward the high cervical region. It was often difficult to detect over the scalp. The last component was best recorded as a positive peak at the scalp and nasopharyngeal electrode. This peak was equivocal when recorded from the cervical region unless an ear reference was used. The latencies and field distributions suggest that the cervical potentials represent a negative field near the generator site and that the scalp recorded potentials are primarily attributable to an approaching field of positivity from the same source. We propose that the possible generator sites of the short latency SEPs are: (1) a distal portion of the brachial plexus (Pc9 and P9), (2) entry to the spinal cord (N11 and P11), (3) cervical cord (N13 and P13), and (4) brain stem or cerebellum (N14 and P14).

Melatonin. A possible role in pathogenesis of adolescent idiopathic scoliosis.

Study Design. The serum melatonin levels during 24‐hour periods were compared between patients with idiopathic and age‐matched normal control subjects. Objective. To find if the melatonin deficiency may have some role for progression or etiology of idiopathic scoliosis in humans. Summary of Background Data. Experimentally induced scoliosis in chicken by pinealectomy can be attributed to the defect in melatonin metabolism. Method. Blood samples were correlated every 3 hours during 24‐hour periods, and serum melatonin levels were measured and statistically analyzed. Results. The level of melatonin, integrated concentration through 24 hours and night time (0:00 AM‐6:00 AM), in the patients who had progressive curve (more than 10° of progression in the previous 12 months) was significantly lower than the level in the patients who had a stable curve (less than 10° of progression in the previous 12 months) or in the control subjects (P<0.05). Conclusion. The study suggests that normal melatonin synthesis or metabolism may have crucial role in regulating normal spine growth. The level of melatonin appears to be a useful predictor for progression of spine curvature in idiopathic scoliosis.

Pathogenesis of idiopathic scoliosis. Experimental study in rats.

STUDY DESIGN A radiographic examination of pinealectomized rats to observe the development of scoliosis and halt the condition by administration of melatonin. OBJECTIVES To discover whether pinealectomy has the same effect in mammals as shown in the chicken, and to determine whether the bipedal condition is important for development of scoliosis. SUMMARY OF BACKGROUND DATA Pinealectomizing chickens shortly after hatching consistently resulted in scoliosis closely resembling human idiopathic scoliosis. It has not been determined whether this phenomenon is restricted solely to chickens, or if this experimental model is applicable to other animals, especially those more closely related to humans. METHODS A sham operation in five bipedal rats served as the control in this study. Pinealectomy was performed in 10 quadrupedal rats, pinealectomy in 20 bipedal rats, and pinealectomy with implantation of melatonin pellet in 10 bipedal rats. Spinal radiographs were used to measure the degree of scoliosis at 3 months after surgery. RESULTS Scoliosis developed only in pinealectomized bipedal rats and not in quadrupedal rats. It developed in none of the sham operation group and in only 1 of 10 pinealectomized bipedal rats with melatonin treatment. CONCLUSIONS Melatonin deficiency secondary to pinealectomy alone does not produce scoliosis if the quadrupedal condition is maintained. The bipedal condition, such as that in chickens or humans, plays an important role in the development of scoliosis. The findings suggest a critical influence of a postural mechanism for the development of scoliosis.

Far‐field somatosensory evoked potentials after stimulation of the tibial nerve

In 21 normal subjects, far-field somatosensory potentials were recorded from the scalp after stimulation of the tibial nerve at the ankle (tibial SEP). With the use of a knee reference contralateral to the side of stimulation, the tibial SEP consisted of three major positive peaks, P17, P24, and P31, and three additional but inconsistent components, P11, P21, and P27. Presumable generator sources of the tibial SEP are the popliteal fossa for P11, entry to the sacral plexus for P17, the cauda equina for P21, entry to the conus medullaris for P24, the rostral spinal cord for P27, and the brainstem for P31.

Topography of somatosensory evoked potentials after stimulation of the median nerve.

We studied topography of major negative-positive peaks, NI, PI, NII, PII and NIII, of scalp recorded somatosensory evoked potentials (SEP) after stimulation of the median nerve. Unlike the diffusely distributed P14, NI, PI and NII recorded from contralateral hemisphere after unilateral stimulation normally showed statistically significant latency increase from frontal (N17, P20, N29) to central (N19, P23, N32) and parietal (N20, P26, N34) electrodes. However, NIII (N60) had considerable inter- and intra-individual variations with no consistent antero-posterior latency shift. In contrast to well localized N19 and N32 peaks at the contralateral central electrode, the N17, P20 and N29 peaks were registered over the bifrontal and ipsilateral central regions as well as in the vertex. The parietal N20 peak was also present at the occipital electrodes bilaterally. In patients with localized cerebral lesions, types of SEP abnormalities varied considerably, presumably reflecting complex somatosensory afferent pathways. A small lesion in posterolateral thalamus may totally eliminate NI, NII and NIII components over both hemispheres, sparing only P14 whereas a sizable lesion in the frontal or parietal lobe may affect only NII or NIII. Capsular lesions spare P14 and frontal N17 but may alter all the subsequent SEP components, or NII or NIII selectively. In some cases, the corresponding peaks at the central and parietal electrodes may be affected independently. The complex relationships between the type of SEP abnormalities and the location of cerebral lesions can best be explained by postulating the presence of multiple, at least partially independent, thalamocortical projections mediating regionally specific somatosensory inputs.

Pathogenesis of idiopathic scoliosis: SEPs in chicken with experimentally induced scoliosis and in patients with idiopathic scoliosis.

We studied somatosensory evoked potentials (SEPs) in 20 chickens with experimentally induced scoliosis after pinealectomy and in 100 patients with idiopathic scoliosis. We also studied 20 chickens without scoliosis and 20 healthy youngsters. In the chickens, SEPs after leg stimulation was significantly delayed in the scoliosis group compared to the controls. In patients, the latency of cortical potential (N37) after stimulation of tibial nerve was longer in the scoliosis group than in the controls. Our findings in both experimental and clinical studies strongly support the hypothesis that idiopathic scoliosis results from dysfunction in the central nervous system. The type of SEPs abnormalities described in idiopathic scoliosis suggest a pathology from the midbrain to the cortex.

Distal slowing of motor nerve conduction velocity in diabetic polyneuropathy

Using the latencies of M response and F wave, motor nerve conduction was assessed along the entire course of the nerve from the spinal cord to the muscle in 102 diabetics and 74 control patients. In diabetics, latencies were increased and conduction velocity decreased over both proximal and distal segments. However, the latency ratio of the proximal to distal segment (F ratio) was slightly but significantly smaller in diabetics (mean +/- SD:0.93 +/- 0.14, 1.35 +/- 0.20, 1.09 +/- 0.19 and 1.02 +/- 0.19 for median, ulnar, tibial and peroneal nerves, respectively) than in control patients (1.05 +/- 0.09, 1.41 +/- 0.12, 1.17 +/- 0.13 and 1.08 +/- 0.12). These findings suggest that motor conduction abnormalities in diabetic polyneuropathy are diffuse over the total length of the nerve, but more intense in the distal than proximal segment. An additional finding in diabetics was that both proximal and distal segments were more frequently affected in the lower than in the upper extremities.

Relation between size of compound sensory or muscle action potentials, and length of nerve segment

In 24 median nerves from 12 healthy subjects, antidromic digital sensory potentials progressively diminished in size, averaging 40.4,37.0, 30.7, and 23.9 μV × msec with stimulation at the palm, wrist, elbow, and axilla, respectively. In contrast, compound muscle action potentials changed minimally, measuring 19.4, 19.8,19.0, and 18.2 mV × msec, respectively. Similar studies of the ulnar and radial nerves showed identical trends. Physiologic temporal dispersion can mimic conduction block of sensory nerves by summating the peaks of opposite polarity generated by fast- and slow-conducting axons. This type of cancellation affects muscle responses much less because motor unit potentials of longer duration superimpose nearly in phase, given the same latency shift as the sensory potentials.